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2016 Fiscal Year Final Research Report

Role of cytidine deaminase in cell reprograming process

Research Project

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Project/Area Number 26460363
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General medical chemistry
Research InstitutionGifu University

Principal Investigator

Nagaoka Hitoshi  岐阜大学, 大学院医学系研究科, 教授 (20270647)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywords再生医学 / DNA脱メチル化
Outline of Final Research Achievements

DNA methylation is one of the major epigenetic mark for gene regulation. Gene expression for DNA demethylation during iPS induction were evaluated. Consistent with previous reports, we failed to detect substantial expression of cytidine deaminases, AID and Apobec1 whereas Tet1 expression was significantly enhanced. Forced expression of AID or Apobec1 under the control of Nanog promoter exhibited no significant effect on iPS induction efficiency and stability at least until up to 60 days after induction. These results suggest minimum role of cytidine deaminases in iPS. These results suggest minimum role of cytidine deaminases in iPS. Hypomethylation at Aicda promoter region in iPS clones may indicate that leaky AID expression could easily occur under certain conditions in which appropriate transcription factors are available. That may explain apparently ambiguous reports for AID expression in iPS.

Free Research Field

分子生物学 分子免疫学

URL: 

Published: 2018-03-22  

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